scholarly journals Transcranial parenhymal sonography in the diagnosis of Parkinson's disease

2008 ◽  
Vol 65 (8) ◽  
pp. 601-605 ◽  
Author(s):  
Milija Mijajlovic ◽  
Igor Petrovic ◽  
Tanja Stojkovic ◽  
Marina Svetel ◽  
Elka Stefanova ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dynamic Range ◽  
Brain Structures ◽  
Transcranial Sonography ◽  
The Body ◽  
Characteristic Finding ◽  
Phased Array Ultrasound ◽  
Array Ultrasound ◽  
The Brain

Bacground/Aim. Modern ultrasound systems allow highresolution transcranial sonography (TCS) of the brain structures. Enlargement of the echogenic signal (hyperechogenicity) of the substantia nigra (SN) has been reported as a highly characteristic finding in idiopathic Parkinson's disease (PD) and is thought to reflect increased amounts of iron, bound to proteins other than ferritin, in the SN in the course of neurodegeneration. The aim of our study was to investigate the prevalence of the SN hyperechogenicity in PD patients, as well as its possible clinical correlates. Methods. The study comprised 103 consecutive PD patients and 50 healthy age-matched controls. For TCS examination a color-coded, phased array ultrasound system equipped with a 2.5 MHz transducer was used (ESAOTE Technos MP, Italia). The examination was performed through a preauricular acoustic bone window with a penetration depth of 16 cm and a dynamic range of 45-50 dB. The SN was identified within the butterfly shaped structure of the mesencephalic brainstem, with scanning from both temporal windows. Results. The SN hyperechogenicity was identified in 95 out of 103 examined PD patients (92%), which was marked in 60 (63%), and moderate in 35 patients (37%). Median SN echogenic size was larger contralateral to the clinically more affected side of the body. Unilateral SN hyperechogenicity was also found in 5 out of 50 healthy controls (10%). No ventricular enlargements were notified in our study. Conclusion. Our study demonstrated SN hyperechogenicity in more than 90% of PD patients. In adult subjects without neurological symptoms, the TCS finding of at least unilaterally marked SN hyperechogenicity indicates a subclinical functional impairment of the nigrostriatal dopaminergic system. .

Comorbidity of normotensive hydrocephalia and Parkinson’s disease

2021 ◽  
Vol 26 (2) ◽  
pp. 30-36
Author(s):  
V. V. Yudina ◽  
O. N. Voskresenskaya ◽  
G. K. Yudina
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Subsequent Development ◽  
The Elderly ◽  
Transcranial Sonography ◽  
History Of ◽  
Clinical Triad ◽  
Gait Disturbances ◽  
The Brain

Normotensive hydrocephalus (NTH) is a syndrome characterized by enlarged ventricles of the brain, gait disturbance, cognitive impairment, and incontinence. In the elderly with gait disturbances of unspecified etiology, NTH should always be excluded. It is especially difficult to diagnose NTH in patients with neurodegenerative diseases, primarily with idiopathic Parkinson’s disease (PD), and vice versa, to diagnose PD in patients with NTH. We report on an 80-year-old patient with a five-year history of NTH, manifested by the classic clinical triad of symptoms and the subsequent development of Parkinson’s syndrome 3 years after the debut of NTH. MRI of his brain revealed ventriculomegaly and transcranial sonography did hyperechogenicity of the substantia nigra on the left, with an area of 0.41 cm2, which made it possible to diagnose two comorbid diseases in the patient, namely, normotensive hydrocephalus and Parkinson’s disease.

Fractionally delineate the neuroprotective function of calbindin-D28k in Parkinson’s disease

2018 ◽  
Vol 11 (08) ◽  
pp. 1850103 ◽  
Author(s):  
Hardik Joshi ◽  
Brajesh Kumar Jha
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dimensional Space ◽  
Cytosolic Calcium ◽  
The Body ◽  
Dopamine Neurons ◽  
Reaction Diffusion Equation ◽  
Substantia Nigra Pars Compacta ◽  
Brain Disorder ◽  
The Brain

Neuron is a fundamental unit of the brain, which is specialized to transmit information throughout the body through electrical and chemical signals. Calcium ([Formula: see text]) ions are known as second messengers which play important roles in the movement of the neurotransmitter. Calbindin-[Formula: see text] is a [Formula: see text] binding protein which is involved in regulation of intracellular [Formula: see text] ions and maintains [Formula: see text] homeostasis level, it also alters the cytosolic calcium concentration ([[Formula: see text]]) in nerve cells to keep the cell alive. Parkinson’s disease (PD) is a chronic progressive neurodegenerative brain disorder of the nervous system. Several regions of the brain indicate the hallmark of the PD. The symptoms of PD are plainly linked with the degeneration and death of dopamine neurons in the substantia nigra pars compacta located in midbrain which is accompanied by depletion in calbindin-[Formula: see text]. In the present paper, the neuroprotective role of calbindin-[Formula: see text] in the cytoplasmic [[Formula: see text]] distribution is studied. The elicitation in [[Formula: see text]] is due to the presence of low amount of calbindin-[Formula: see text] which can be portrayed and is a hallmark of PD. A one-dimensional space time fractional reaction diffusion equation is designed by keeping in mind the physiological condition taking place inside Parkinson’s brain. Computational results are performed in MATLAB.

scholarly journals TLR2 and TLR4 in Parkinson’s disease pathogenesis: the environment takes a toll on the gut

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Anastazja M. Gorecki ◽  
Chidozie C. Anyaegbu ◽  
Ryan S. Anderton
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Intestinal Barrier ◽  
The Body ◽  
Enteric Neurons ◽  
Gut Dysfunction ◽  
Gut Homeostasis ◽  
The Brain

AbstractParkinson’s disease (PD) is an incurable, devastating disorder that is characterized by pathological protein aggregation and neurodegeneration in the substantia nigra. In recent years, growing evidence has implicated the gut environment and the gut-brain axis in the pathogenesis and progression of PD, especially in a subset of people who exhibit prodromal gastrointestinal dysfunction. Specifically, perturbations of gut homeostasis are hypothesized to contribute to α-synuclein aggregation in enteric neurons, which may spread to the brain over decades and eventually result in the characteristic central nervous system manifestations of PD, including neurodegeneration and motor impairments. However, the mechanisms linking gut disturbances and α-synuclein aggregation are still unclear. A plethora of research indicates that toll-like receptors (TLRs), especially TLR2 and TLR4, are critical mediators of gut homeostasis. Alongside their established role in innate immunity throughout the body, studies are increasingly demonstrating that TLR2 and TLR4 signalling shapes the development and function of the gut and the enteric nervous system. Notably, TLR2 and TLR4 are dysregulated in patients with PD, and may thus be central to early gut dysfunction in PD. To better understand the putative contribution of intestinal TLR2 and TLR4 dysfunction to early α-synuclein aggregation and PD, we critically discuss the role of TLR2 and TLR4 in normal gut function as well as evidence for altered TLR2 and TLR4 signalling in PD, by reviewing clinical, animal model and in vitro research. Growing evidence on the immunological aetiology of α-synuclein aggregation is also discussed, with a focus on the interactions of α-synuclein with TLR2 and TLR4. We propose a conceptual model of PD pathogenesis in which microbial dysbiosis alters the permeability of the intestinal barrier as well as TLR2 and TLR4 signalling, ultimately leading to a positive feedback loop of chronic gut dysfunction promoting α-synuclein aggregation in enteric and vagal neurons. In turn, α-synuclein aggregates may then migrate to the brain via peripheral nerves, such as the vagal nerve, to contribute to neuroinflammation and neurodegeneration typically associated with PD.

scholarly journals Magnetic resonance morphometry of the brain in the advanced stages of Parkinson's disease and vascular parkinsonism

2021 ◽  
Vol 11 (4) ◽  
pp. 16-22
Author(s):  
E. V. Iskhakova ◽  
A. G. Trufanov ◽  
A. Yu. Efimtsev ◽  
A. A. Yurin ◽  
A. S. Lepekhina ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Differential Diagnosis ◽  
Magnetic Resonance ◽  
Brain Structures ◽  
Pathological Process ◽  
Vascular Parkinsonism ◽  
Stage 4 ◽  
Advanced Stages ◽  
The Brain

Introduction. MR-morphometry is a method of image processing independent of the researcher, which allows you to get the results of measuring the volume of the brain structures and the thickness of various areas of the cortex and helps in the differential diagnosis in assessing the results of MRI. Our study used MR-morphometry to identify structural markers in the differential diagnosis of vascular parkinsonism in the examination of patients with Parkinson's symptoms. Purpose of research. Visualization of the distribution of atrophic changes in brain structures in vascular parkinsonism and in the advanced stages of Parkinson's disease, as well as the identification of characteristic parts of the brain that undergo a pathological process to increase the accuracy of differential diagnosis. Materials and methods. The results of magnetic resonance morphometry of patients using the postprocessing of native MR images using Freesurfer software are analyzed. We examined 29 patients with vascular parkinsonism and 19 patients with Parknison disease, at stage 4 according to Hyun and Yar. Summary. The application of the method of postprocessing data processing of MR-morphometry allows instrumental confirmation of the clinical diagnosis, as well as to clarify the pathogenesis of neurological syndromes observed in progressive supranuclear paralysis.

scholarly journals Early Parkinson’s Disease-Like Pathology in a Transgenic Mouse Model Involves a Decreased Cst3 mRNA Expression But Not Neuroinflammatory Response in the Brain

2020 ◽  
Vol 3 (2) ◽  
pp. 66-78
Author(s):  
T.A. Korolenko ◽  
A.B. Shintyapina ◽  
V.M. Belichenko ◽  
A.B. Pupyshev ◽  
A.A. Akopyan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Transgenic Mice ◽  
Cystatin C ◽  
Brain Structures ◽  
Cysteine Protease Inhibitor ◽  
Mrna Levels ◽  
Protein Clearance ◽  
Significant Difference ◽  
The Brain

AbstractPathological aggregation and accumulation of α-synuclein in neurons play a core role in Parkinson’s disease (PD) while its overexpression is a common PD model. Autophagy-lysosomal pathways are general intraneural mechanisms of protein clearance. Earlier a suppressed autophagy in the brain of young transgenic mice overexpressing the А53Т-mutant human α-synuclein (mut(PD)) was revealed. Previous studies have recognized that Cystatin C displays protective activity against neurodegeneration. This cysteine protease inhibitor attracts particular attention as a potential target for PD treatment related to autophagy modulation. Here we evaluated the mRNA levels of Cst3 encoding Cystatin C in different brain structures of 5 m.o. mut(PD) mice at standard conditions and after the chronic treatment with a neuroprotective agent, ceftriaxone (100 mg/kg, 36 days). The inflammatory markers, namely, microglial activation by IBA1 expression and mRNA levels of two chitinases genes (Chit1, Chia1), were also assessed but no significant difference was found between control and transgenic mice. Cst3 mRNA levels were significantly reduced in the striatum and amygdala in the transgenic PD model. Furthermore, this was associated with autophagy decline and might be added to early signs of synucleinopathy development. We first demonstrated the modulation of mRNA levels of Cst3 and autophagy marker Becn1 in the brain by ceftriaxone treatment. Taken together, the results support the potential of autophagy modulation through Cystatin C at early stages of PD-like pathology.

scholarly journals Transcranial sonography as a diagnostic tool for Parkinson's disease: a pilot study in the city of Rio de Janeiro, Brazil

2011 ◽  
Vol 69 (6) ◽  
pp. 892-895 ◽  
Author(s):  
Rita de Cássia Leite Fernandes ◽  
Ana Lucia Zuma de Rosso ◽  
Maurice Borges Vincent ◽  
Kátia Silveira da Silva ◽  
Claudia Bonan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Brain Structures ◽  
Transcranial Sonography ◽  
Current Data ◽  
Brazilian Sample ◽  
Sample Method ◽  
The City ◽  
Temporal Windows ◽  
Deep Brain

In Brazil there is no systematic study on Transcranial Sonography (TCS), a neuroimaging method that depicts echogenic deep brain structures using ultrasound. OBJECTIVE: To establish the percentage of subjects with permissive temporal windows and to address the ability of TCS of the substantia nigra (SN) to distinguish parkinsonian patients in a Brazilian sample. METHOD: We performed TCS using the Acuson X300 (Siemens, Germany) in 37 individuals: 23 with Parkinson's disease (PD) and 14 healthy controls. RESULTS: 10.8% of subjects had insufficient temporal acoustic bone windows. SN echogenic areas were larger in patients (mean±SD, 0.31±0.08cm²) compared to controls (mean±SD, 0.17±0.02cm²). TCS accurately identified 88.2% of PD patients. CONCLUSION: A large proportion of Brazilians seem to be eligible for TCS. An expressive number of PD patients could be diagnosed by TCS based on an expanded SN echogenic area. However, the current data is preliminary and must be corroborated by larger studies.

scholarly journals MICROBIOTA INTESTINAL RELACIONADA A DOENÇA DE PARKINSON

2021 ◽  
Vol 5 (1) ◽  
pp. 49-60
Author(s):  
Caroline Felix da Silva ◽  
Graziele Estevo Azevedo ◽  
Natália Franco Taketani
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Gastrointestinal Tract ◽  
Intestinal Microbiota ◽  
Direct Relationship ◽  
Progressive Disease ◽  
Signs And Symptoms ◽  
The Body ◽  
Early Age ◽  
The Brain

RESUMO. A Doença de Parkinson é uma doença crônica, neurodegenerativa e progressiva onde não tem cura. Ainda há muitas investigações para se descobrir a causa da patologia. Em estudos recentes descobriram que pode ter uma relação direta com intestino, com a possibilidade de origem na microbiota intestinal e espalhando-se até o cérebro, com relação a uma desregulação no trato gastrointestinal. É reconhecido que, antes de aparecer os sinais e sintomas motores da doença, o organismo começa a sofrer alterações desde cedo, como a constipação intestinal, com o fortalecimento da hipótese de que a doença de Parkinson tenha início no trato gastrointestinal, e chegue até o cérebro através do nervo vago. Este trabalho pretende abordar sobre a microbiota intestinal e a sua conexão com a doença de Parkinson fazendo revisão de estudos e evidência de como sua composição no hospedeiro pode influenciar o seu metabolismo. A modulação da microbiota intestinal poderá, então, ser uma estratégia para o desenvolvimento de novas opções terapêuticas para o tratamento de doenças neurodegenerativas. ABSTRACT. Parkinson's Disease is a chronic, neurodegenerative and progressive disease that has no cure. There are still many investigations to discover the cause of the pathology. In recent studies they found that it may have a direct relationship with the intestine, with the possibility of originating in the intestinal microbiota and spreading to the brain, with respect to dysregulation in the gastrointestinal tract. It is recognized that, before the appearance of the motor signs and symptoms of the disease, the body begins to undergo changes from an early age, such as intestinal constipation, with the strengthening of the hypothesis that Parkinson's disease starts in the gastrointestinal tract and reaches the brain through the vagus nerve. This work intends to approach the intestinal microbiota and its connection with Parkinson's disease, reviewing studies and evidence on how its composition in the host can influence its metabolism. The modulation of the intestinal microbiota could then be a strategy for the development of new therapeutic options for the treatment of neurodegenerative diseases.

Which Drug for Parkinsonism? Walking, Stiffness, Tremor, and Slowness

2013 ◽  
Author(s):  
J. Eric Ahlskog
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Substantia Nigra ◽  
The Body ◽  
Brain Dopamine ◽  
Arm Swing ◽  
Repetitive Movements ◽  
The Brain ◽  
Repetitive Motor

In Chapters 1 and 4, we briefly summarized the symptoms of parkinsonism. Parkinsonism implies movement problems that are typical of Parkinson’s disease. They remain treatment issues during the lifetime of people with Parkinson’s disease, even if dementia develops. Similarly, parkinsonism also typically occurs in DLB, although to variable degrees. In these disorders parkinsonism primarily reflects low brain dopamine levels and improves with dopamine replacement therapy, often markedly. Parkinsonism occurs when a region of the brain called the basal ganglia ceases to work properly (see Figure 4.2 in Chapter 4). As discussed in Chapter 4, the substantia nigra is a crucial regulator of basal ganglia activity, which is mediated by dopamine release in the striatum. The substantia nigra degenerates in these Lewy disorders and, as a result, brain dopamine declines. With a decline in dopamine, movement slows. Bradykinesia is the medical term for such slowness. This manifests as not only slowed movement but also less movement and smaller than normal movements. Unconscious automatic movements, such as blinking or arm swing, diminish. A unique tremor of the hands (sometimes legs) often develops when these limbs are in a relaxed position (rest tremor). For unknown reasons, the brain is not affected symmetrically, hence, neither is the body. Typically, one side of the body is much more impaired than the other. The extent to which these symptoms develop differs from person to person and includes various combinations of the following components. The slowness may be apparent on one or both sides of the body. For example, one leg may lag behind when walking. The overall appearance is characterized by moving much slower than expected for one’s age. The person feels as if they are moving in molasses—everything slows down. Many of our daily activities involve repeated small movements, such as writing or brushing teeth. In the Lewy conditions of DLB and PDD, the size (amplitude) of repetitive movements diminishes, impairing the activity. This is exemplified by the small handwriting of someone with parkinsonism, termed micrographia. Clinicians assess repetitive motor function by asking the patient to repetitively tap the thumb and index finger.

scholarly journals Physical therapy of the early non-motorized violations to slow the progression of Parkinson's disease

2019 ◽  
pp. 117-120
Author(s):  
А. I. Labinskiy ◽  
G. B. Labinska
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Physical Therapy ◽  
The Body ◽  
Motor Symptoms ◽  
Physical Treatment ◽  
Treatment Regimens ◽  
Objective State ◽  
Non Motor Symptoms ◽  
The Brain

The authors developed and applied the original complex of innovative combined physical therapy of non-motor manifestations of the early stages of Parkinson's disease to slow its progression. Applied concomitant treatments affect some parts of the etiology and pathogenesis of non-motor manifestations of Parkinson's disease. In particular, hirudotherapy restores the rheological properties of blood without side effects characteristic of known anticoagulants; helps to restore tissue trophism, in particular the brain. Nutritional correction prevents the development of digestive disorders. The main principles of such nutrition were: 1. The role of antioxidant saturation of the diet for the correction of metabolism. 2. The value of increasing the number of "ballasts" in the diet. 3. "Free mode" of food intake (at the request of the organism), taking into account the human biorhythms (daily, seasonal and psychological). 4. The need for periodic short-term fasting - as a method of cleansing the body. 5. The need for separate power. Manual therapy in the variant proposed by the authors prevents the vertebral component of the destructive processes in the brain. After the use of combined physical therapy, an improvement in the objective state of patients with Parkinson's disease was noted. According to the study, non-motor symptoms on the scale of autonomic disorders and non-motor symptoms (NMSS) were statistically significantly less pronounced in all patients examined in the group of patients using the developed complex of physical therapy compared to the group of patients without using the developed complex of physical therapy. Considering the improvement of the objective state of patients after the applied physical treatment, we can recommend the indicated therapeutic technique for the complex treatment of early non-motor manifestations of Parkinson's disease, slowing its progression and improving the effectiveness of existing modern treatment regimens of the studied pathology.

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